Salidroside induced repair of myocardial infarction through Nrf2/HO-1

Authors

  • Yanbo Fan Department of Cardiology, Wuhan Hospital of Traditional Chinese Medicine, Wuhan 430014, Hubei, China
  • Wei Wang Department of Cardiology, Wuhan Hospital of Traditional Chinese Medicine, Wuhan 430014, Hubei, China
  • Liqun Tian Department of Cardiology, Wuhan Hospital of Traditional Chinese Medicine, Wuhan 430014, Hubei, China
  • Jie Yin Department of Cardiology, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, PR China

DOI:

https://doi.org/10.1590/s2175-97902022e20218%20%20

Keywords:

Fibrosis, HO-1, Myocardial Infarction, Salidroside, PI3K/Akt

Abstract

Salidroside (SAL) has been confirmed to have some protective effects against inflammatory injury. However, little information was established as to the mechanism of these protective effects. To this effect, we designed this study to explore the protective effects and mechanisms of SAL against myocardial infarction (MI). A rat MI model was established and divided into five groups (n = 6): sham, MI, MI+SAL, MI+ LY294002 (PI3K inhibitor), and MI+SAL+ LY294002. The cardiac function and histological pathology were analyzed with a color Doppler ultrasonic diagnostic instrument. Anti-oxidative enzyme activities and the production of inflammatory media were assayed by biochemical kits and ELISA. MI size and fibrosis were assayed by Masson’s trichrome staining while Bax/Bcl-2 and PI3K/Akt/Nrf2/HO-1 were assayed by Western blotting and immunofluorescence. The results showed that SAL significantly improved the left ventricle ejection fraction and fractional shortening, decreased the MI size and fibrosis, inhibited apoptosis and promoted blood vessel formation. SAL promoted anti-oxidative and anti-inflammatory abilities. Moreover, SAL enhanced PI3K/ Akt/Nrf2/HO-1 expression. To this effect, we designed this study suggested that SAL induced repair of MI via PI3K/A kt/ Nrf2/HO-1.

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References

Bajinka O, Tan Y, Abdelhalim KA, Özdemir G, Qiu X.Extrinsic factors influencing gut microbes, the immediate consequences and restoring eubiosis. AMB Express. 2020;10(1):130.

Fiorelli S, Porro B, Cosentino N, Di Minno A, Manega CM, Fabbiocchi F, et al. Activation of Nrf2/HO-1 pathway and human atherosclerotic plaque vulnerability: an in vitro and in vivo study. Cells. 2019;8(4):pii: E356.

Kishimoto Y, Ibe S, Saita E, Sasaki K, Niki H, Miura K, et al. Plasma heme oxygenase-1 levels in patients with coronary and peripheral artery diseases. Dis Markers. 2018;2018:6138124.

Li L, Liu M, Kang L, Li Y, Dai Z, Wang B, et al. HHEX: A crosstalker between HCMV infection and proliferation of VSMCs. Front Cell Infect Microbiol. 2016;6:169.

Lin X, Bai D, Wei Z, Zhang Y, Huang Y, Deng H, et al. Curcumin attenuates oxidative stress in RAW264.7 cells by increasing the activity of antioxidant enzymes and activating the Nrf2-Keap1 pathway. PLoS One. 2019;14(5):e0216711.

Loginov VI,Pronina IV,Burdennyi AM,Pereyaslova EA,Braga EA,Kazubskaya TP, et al. Role of methylation in the regulation of apoptosis genes APAF1, DAPK1, and BCL2 in breast cancer. Bull Exp Biol. 2017;162(6):797-800.

Liu X, Pachori AS, Ward CA, Davis JP, Gnecchi M, Kong D, et al. Heme oxygenase-1 (HO-1) inhibits postmyocardial infarct remodeling and restores ventricular function. FASEB J. 2006;20(2):207-16.

Lu H, Li Y, Zhang T, Liu M, Chi Y, Liu S, et al. Salidroside reduces high-glucose-induced podocyte apoptosis and oxidative stress via upregulating heme oxygenase-1 (HO-1) expression. Med Sci Monit. 2017;23:4067-76.

Montalescot G, Bolognese L, Dudek D, Goldstein P, Hamm C, Tanguay JF, et al. Pretreatment with prasugrel in non-ST-segment elevation acute coronary syndromes. N Engl J Med. 2013;369(11):999-1010.

Pu WL, Zhang MY, Bai RY, Sun LK, Li WH, Yu YL, et al. Anti-inflammatory effects of Rhodiola rosea L.: A review. Biomed Pharmacother. 2020;121:109552.

Sun Y, Xun L, Jin G, Shi L. Salidroside protects renal tubular epithelial cells from hypoxia/reoxygenation injury in vitro. J Pharmacol Sci. 2018;137(2):170-6.

Varenne O, Cook S, Sideris G, Kedev S, Cuisset T, Carrié D, et al. Drug-eluting stents in elderly patients with coronary artery disease (SENIOR): a randomised single-blind trial. Lancet. 2018;391(10115):41-50.

Wang J, Pan Y, Cao Y, Zhou W, Lu J. Salidroside regulates the expressions of IL-6 and defensins in LPS-activated intestinal epithelial cells through NF-κB/MAPK and STAT3 pathways. Iran J Basic Med Sci. 2019;22(1):31-7.

Wang X, Saud SM, Zhang X, Li W, Hua B. Protective effect of shaoyao decoction against colorectal cancer via the Keap1-Nrf2-ARE signaling pathway. J Ethnopharmacol. 2019;241:111981.

Yu Y, Yang Y, Yang M, Wang C, Xie K, Yu Y. Hydrogen gas reduces HMGB1 release in lung tissues of septic mice in an Nrf2/HO-1-dependent pathway. Int Immunopharmacol. 2019;69:11-8.

Zhao X, Lu Y, Tao Y, Huang Y, Wang D, Hu Y, et al. Salidroside liposome formulation enhances the activity of dendritic cells and immune responses. Int Immunopharmacol . 2013;17(4):1134-40.

Zhong Z, Han J, Zhang J, Xiao Q, Hu J, Chen L. Pharmacological activities, mechanisms of action, and safety of salidroside in the central nervous system. Drug Des Devel Ther. 2018;12:1479-89.

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Published

2022-12-23

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Section

Original Article

How to Cite

Salidroside induced repair of myocardial infarction through Nrf2/HO-1. (2022). Brazilian Journal of Pharmaceutical Sciences, 58. https://doi.org/10.1590/s2175-97902022e20218